An experimental model found that VEGF-A enhanced HCC proliferation by interacting with VEGFR-1 and VEGFR-2, and that treatment of high VEGFR-1/2-expressing HepG2 cells with sorafenib, an inhibitor targeting several kinases including VEGFRs, inhibited cell proliferation, reduced VEGFR-2 mRNA expression in vitro, and delayed xenograft tumor growth in vivo [32]. The gene discussed is KDR; the disease is neoplasm.